Fig. 7: Spontaneous waves reflect structured fluctuations in E/I balance that sparsely modulate spike probability.

a Membrane voltage for a simulated neuron in either the sparse-wave network (black line) or dense-wave network (purple line) calculated from the summed excitatory and inhibitory synaptic currents received by that neuron. Spiking activity occurred when the voltage crosses the threshold (Vth red line). The distribution of membrane potentials over the interval for the sparse and dense networks is plotted on the right. b The amplitude of the simulated LFP (blue line) and the relative level of excitatory and inhibitory conductance (red line) over a 10 × 10 neuron pool were counter phase. c Scatter plot of LFP and ge − gi difference revealed a significant negative correlation (N = 50,000 time points; Pearson’s r = −0.83; CI test, α = 0.01). d Spike-phase coupling was significant across networks in the asynchronous-irregular regime, and the degree of coupling was correlated with the magnitude of synaptic conductance (N = 599 simulations; Pearson’s r = 0.78 ± 0.001, 95% CI). e Histogram showing the fraction of spikes that occurred during each phase of the simulated LFP in the topographically connected network. Spike probability was modulated by the LFP phase (N = 22 resamples vs. shuffle; spike-phase index = 0.15). f Same as in (e), but for recorded cortical data. Spike probability was similarly modulated (spike-phase index = 0.16; N = 22 recording sessions vs. shuffle). g The dense-wave network simulation had a significantly stronger spike-phase relationship (N = 10 resamples; spike-phase index = 0.44, p = 0.0000085, two-tailed Wilcoxon’s rank-sum test).